Thalamocortical relations in taste aversion learning: II. Involvement of the medial ventrobasal thalamic complex in taste aversion learning

Abstract

Previous neurobehavioral studies have implicated the gustatory thalamocortical relay as a functional substrate of conditioned taste aversion (CTA) learning. These experiments were conducted to examine the involvement of the gustatory thalamic nuclei in fundamental taste reactivity, gastrointestinal reactivity, and CTA learning. In Experiment 1, bilateral electrolytic lesions were produced in the medial ventrobasal thalamic complex (VBm), including the thalamic gustatory nuclei, in one group of rats. A separate group of rats received control lesion placements in the mediodorsal-periventricular (MD-PV) thalamic nuclei. Animals then received preference-aversion taste tests followed by CTA conditioning. At the conclusion of conditioning, lesions were produced in the anterior insular gustatory neocortex (AIGN) to evaluate whether or not the AIGN contributed to CTA learning in animals lacking VBm thalamus. Results of Experiment 1 indicated that control lesions did not disrupt taste reactivity, gastrointestinal reactivity, or CTA learning. Destruction of VBm thalamus attenuated taste reactivity to sucrose, citric acid, and quinine hydrochloride; however, such lesions did not impair normal taste reactivity to sodium chloride. Lesion placements in VBm thalamus also did not reliably impair gastrointestinal reactivity to ingested LiCl. Elimination of VBm thalamus markedly attenuated CTA learning. Results of neocortical lesion manipulations showed that the AIGN contributed to initial CTA learning in animals lacking MD-PV thalamus but that the AIGN did not mediate initial CTA learning in animals lacking VBm thalamus. Whether animals lacking VBm thalamus used olfactory cues associated with drinking solutions to acquire CTAs was evaluated in Experiment 2. Results of Experiment 2 demonstrated that animals lacking VBm thalamus and the olfactory bulbs could not acquire aversions to ingested LiCl following eight conditioning trials. These experiments demonstrate that destruction of VBm thalamus, including the gustatory thalamic nuclei, is sufficient to prevent CTA learning.